BET bromodomain inhibitors attenuate transcription of a subset of IL-1-induced NF-κB targets that promote inflammation in β-cells.

ABSTRACT: Cytokine-stimulated transcription of NF-κB target genes is linked to the development of multiple inflammatory and autoimmune diseases. Inhibitors of bromodomain and extraterminal domain (BET) epigenetic reader proteins attenuate inflammatory gene transcription and delay the onset of several inflammatory diseases, including autoimmune diabetes. Our previous studies showed that BET bromodomain inhibitors disrupt the interaction between BET family member BRD4 and NF-κB transcription factor p65 in β-cells, thus attenuating cytokine-stimulated NF-κB-dependent gene and functional changes. However, the role of NF-κB in developing inflammatory disease is controversial, as NF-κB inhibition can promote disease progression in some contexts. NF-κB target genes play both physiological and pathophysiolo

SUBMITTER: Nord JA 

PROVIDER: S-EPMC12270673 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature